Angiogenesis, the process of the formation of new blood vessels from pre-existing capillaries, is required for the sustained growth, invasion and spread of tumors. Thus, the inhibition of tumor angiogenesis has been considered to be one of the important targets in anticancer therapy. Utilizing cDNA microarray analysis, it has been demonstrated that the expression of genes such as DOC1, KLF4 and TC-1 was rapidly modulated by the angiogenesis inhibitors, endostatin and fumagillin. In addition, DOC1 (downregulated in ovarian cancer 1; also known as FILIP1L (filamin A interacting protein 1-like)) was shown to be an upstream regulator of KLF4 and TC-1 following endostatin treatment (Mazzanti C M et al. Genome Res (2004) 14:1585). Expression of DOC1 was rapidly regulated by another angiogenesis inhibitor EMAP II (Tandle A T et al. Cytokine (2005) 30:347). DOC1 mRNA expression has been shown to be consistently absent in ovarian carcinoma cells (Mok S C et al. Gynecol Oncol (1994) 52:247). In addition, it has been shown to be induced in senescent human prostate epithelial cells, but significantly repressed in immortalized prostate epithelial cells (Schwarze S R et al. J Biol Chem (2002) 277:14877; and Schwarze S R et al. Neoplasia (2005) 7:816). Furthermore, DOC1 mRNA expression was shown to be downregulated in microvascular endothelial cells infected with Kaposi's sarcoma-associated herpesvirus as well as during B-cell transformation (Poole L I et al. J Virol (2002) 76:3395 7; and Klener P et al. J Virol (2006) 80:1922). The function of DOC1, however, is completely unknown.